A possible mechanism for interaction of environmental carcinogens such as hydrocarbon emissions may be specific or non-specific deleterious effects on immunoregulation during chemical carcinogenesis. Treatment of C3H mice with 1.0 or 0.05 mg of 3-methylcholanthrene (3-MC) has been found to result in acceleration of growth of transplanted syngeneic fibrosarcomas. Use of 1.0 mg 3-MC induced greater facilitation of tumor growth than did 0.05 mg 3-MC. However, treatment of mice with 0.05 mg 3-MC also facilitated growth of two transplanted tumors. This lower dose of 3-MC induced primary tumors in only 50% of injected mice. The purpose of this study is to further investigate the immunobiology of 3-MC induced facilitation of syngeneic tumor growth. The study will determine if the effect is (a) due to immunosuppression, (b) transferable to a syngeneic recipient, (c) immunologically mediated, (d) a general phenomenon or demonstrable with only occasional tumors, and (e) observed during chronic administration of split doses of carcinogen. The study will determine the effect on 1.0 mg and 0.05 mg 3-MC on the hemolysin plaque assay, skin graft rejection, lymphocyte mitogen stimulation, in vitro tumor cytotoxicity, macrophage phagocytic function, and mixed lymphocyte culture 1, 4, 8, and 12 weeks after carcinogen treatment. To test whether carcinogen induced acceleration of tumor growth is transferable to syngeneic recipients and immunologically mediated, the techniques of parabiosis, passive transfer of spleen and lymph node cells, and passive transfer of serum will be used. In addition the effect of carcinogen on second set tumor rejection will be investigated. Tumors of both low and moderate immunogenicity will be used to challenge mice which are carcinogen treated. This will determine if acceleration of tumor growth is specific to some tumors or demonstrable with all tumors.